Organ Size Determination Research Articles

19-P010 Head-regeneration through cell death and compensatory proliferation in the Hydra

cells along the proximodistal (PD) axis concomitantly with remodelling of the pre-existing stump, making the regenerated legs shorter than normal. In contrast, knockdown of the expanded (ex) or Merlin (Mer) transcripts induced over-proliferation of the regenerating cells, making the regenerated legs longer. These results are consistent with those obtained using rdRNAi during intercalary regeneration induced by leg transplantation. Since these findings fit well with the Ds/Ft steepness model for the determination of organ size, we propose the following model for the control of leg regeneration. A Ds/Ft gradient is responsible for sensing positional disparity and driving proliferation of regenerating cells by activation of the Hippo/Warts pathway. The leg size of regenerates is determined by the steepness of the Ds/Ft gradient, such that growth ceases when the slope of the linear gradient falls below a certain threshold value, which may be determined by an Ex/Mer interaction. Our findings provide additional insight into the longstanding question of how the size and shape of an appendage is determined in metazoa.

The biology of organ size determination

The mechanisms that control the size of cells, organs, and organisms have long interested biologists, and are also important in malignant progression. Despite this, basic features of in vivo growth control - the level at which regulation is exerted and the degree to which size is controlled autonomously - are poorly understood. Similarly, it is unknown whether adult tissues measure and respond to size cues in the same manner as those of embryos, a question that is relevant to tissue homeostasis and regeneration. This article will review the determinants of organ size during development and discuss the concept of a 'size set-point,' which incorporates the mass of tissue parenchyma and scaffold established at the end of development.

Drosophila genetic variants that change cell size and rate of proliferation affect cell communication and hence patterning

We explore in this paper the role of genetic variants that affect cell size and proliferation in the determination of organ size. We use genetic mosaics of loss or gain of function in six different loci, which promotes smaller or larger than normal cells, associated to either smaller or larger than normal territories. These variants have autonomous effects on patterning and growth in mutant territories. However, there is no correlation between cell size or rate of proliferation on the size of the mutant territory. In addition, these mosaics show non-autonomous effects on surrounding wildtype cells, consisting always in a reduction in number of non-mutant cells. In all mutant conditions the final size (and shape) of the wing is different than normal. The phenotypes of the same variants include higher density of chaetae in the notum. These autonomous and non-autonomous effects suggest that the control of size in the wing is the result of local cell communication defining canonic distances between cells in a positional-values landscape.

Effect of organ and tissue masses on resting energy expenditure in underweight, normal weight and obese adults.

In normal-weight subjects, resting energy expenditure (REE) can be accurately calculated from organ and tissue masses applying constant organ-specific metabolic rates. This approach allows a precise correction for between-subjects variation in REE, explained by body composition. Since a decrease in organ metabolic rate with increasing organ mass has been deduced from interspecies comparison including human studies, the validity of the organ- and tissue-specific REE calculation remains to be proved over a wider range of fat-free mass (FFM). In a cross-sectional study on 57 healthy adults (35 females and 22 males, 19-43 y; 14 underweight, 25 intermediate weight and 18 obese), magnetic resonance imaging (MRI) and dual-energy X-ray absorptiometry (DXA) were used to assess the masses of brain, internal organs, skeletal muscle (MM), bone and adipose tissue. REE was measured by indirect calorimetry (REEm) and calculated from detailed organ size determination by MRI and DXA (REEc1), or in a simplified approach exclusively from DXA (REEc2). We found a high agreement between REEm and REEc1 over the whole range of FFM (28-86 kg). REE prediction errors were -17 +/- 505, -145 +/- 514 and -141 +/- 1058 kJ/day in intermediate weight, underweight and obese subjects, respectively (n.s.). Regressing REEm on FFM resulted in a significant positive intercept of 1.6 MJ/day that could be reduced to 0.5 MJ/day by adjusting FFM for the proportion of MM/organ mass. In a multiple regression analysis, MM and liver mass explained 81% of the variance in REEm. DXA-derived REE prediction showed a good agreement with measured values (mean values for REEm and REEc2 were 5.72 +/- 1.87 and 5.82 +/- 1.51 MJ/day; difference n.s.). Detailed analysis of metabolically active components of FFM allows REE prediction over a wide range of FFM. The data provide indirect evidence for a view that, for practical purposes within humans, the specific metabolic rate is constant with increasing organ mass. Nonlinearity of REE on FFM was partly explained by FFM composition. A simplified REE prediction algorithm from regional DXA measurements has to be validated in future studies.

Sonographic visualization and size determination of the abdominal organs in healthy newborn infants

The determination of organ size is another important criterium in ultrasound examination. There are only few investigations in the neonatal group. Therefore in a prospective study the abdominal organs of 85 neonates were examined with a 7.5 MHz small part scanner. These organs were measured in standardized sections in order to establish normal values]

On the Nature of Hereditary Size Limitation

ABSTRACT If it could be shown that the determination of organ size in the animal body is not reached by an independent process, but that the magnitude of any one structure is determined by that of others, such evidence, if of a strictly quantitative nature, would tend to affirm the existence of a physical mechanism regulating the relative growth of body components. It is the object of this paper to present such evidence, and to describe a model from physical chemistry which lends a reasonable interpretation to the diversification observed in the ontogenetic and phylogenetic history of organ size.